Inflammatory bowel disease (IBD) encompasses several chronic inflammatory conditions, most significantly ulcerative colitis (UC) and Crohn's disease (CD). While these two conditions share many common features—diarrhea, bloody stools, weight loss, abdominal pain, fever, and fatigue—each has unique features. A complete discussion of Crohn's disease will be addressed in a future article. Ulcerative colitis and associated risk factors, pathogenesis, nutrient deficiencies, conventional treatment approaches, natural treatment approaches, and extra-intestinal manifestations of the disease.
Ulcerative colitis affects the colon and rectum and typically involves only the innermost lining or mucosa, manifesting as continuous areas of inflammation and ulceration, with no segments of normal tissue. The Crohn's and Colitis Foundation of America defines several varieties of UC. Disease involving only the most distal part of the colon and the rectum is termed ulcerative proctitis; disease from the descending colon down is referred to as limited or distal colitis; and disease involving the entire colon is called pancolitis. UC may be insidious, with gradual onset of symptoms, or the first attack may be acute and fulminate.
More mild symptoms include a progressive loosening of the stool, abdominal cramping, and diarrhea. As the disease progresses from mild to more severe, the patient may also experience weight loss, fatigue, loss of appetite that may result in nutrient deficiencies, mucus in the stool, severe rectal bleeding, fever, and anemia. It is estimated that 1-2 million Americans suffer from IBD; approximately half of these have ulcerative colitis. UC can occur anytime in life, but is usually diagnosed prior to age 30. The disease appears to affect men and women equally. Approximately 20 percent of people with UC have a close relative with IBD. Caucasians have a higher incidence of UC, with Jewish people of European descent 3-6 times more likely to develop the disease. Regions with a low incidence of UC include Asia, Japan, Africa, and South America.
Differing cytokine and other inflammatory-mediator profiles have been identified for UC and CD. The classic lesions of UC, involving the mucosal layer with extensive epithelial damage, abundant neutrophils, and crypt abscesses have led to a search for an immune mechanism to explain the epithelial damage. Signs of increased oxidative stress are in evidence in the intestinal mucosa of patients with ulcerative colitis and may be secondary to inflammation. One study examined signs of oxidative stress and plasma antioxidant levels in controls compared to patients with UC and CD. Oxidative DNA damage was noted in both IBD groups compared to controls, measured by production of 8-hydroxy-deoxyguanosine (8-OHdG). UC patients were found to have significantly lower plasma levels of vitamins A and E and several carotenoids compared to controls; there were no differences between UC and CD groups.
Mucosal biopsies of UC patients were analyzed and shown to have increased reactive oxygen intermediates, DNA oxidation products (8-OHdG), and iron in inflamed tissue compared to controls. Decreased levels of copper and zinc, cofactors for the endogenous antioxidant superoxide dismutase, were also observed.
Managing acute pathology of often relies on the addressing underlying pathology and symptoms of the disease. There is currently a need in the art for new compositions to treatment or delay of the onset of Inflammatory Bowel Disease and its associated complications progression.